We hypothesize that cell mediated immunity (CMI) plays an important role in the development of experimental glomerulonephritis (GN) and GN in man. We plan to study this using an animal model of humorally deficient chickens that develop GN in the absence of deposition of antibody. This nephritis appears identical to that in normal chickens with antibody deposits in glomeruli. The specific aims include further refinement of the model in inbred lines of chickens so that transfer of cells can be accomplished without graft vs host reaction. We plan to further define the dosing interval of the antigen, the type of antigen, and the amount of antigen which gives the most florid disease. We will be using endogenous auto-antigens without implantation of exogenous antigens to induce the disease. Thereafter, adoptive transfer studies will be performed to attempt to delineate which cells might be involved and to show that disease can be transferred with cells. The results of these studies provide major information regarding the role of CMI in the development of experimental nephritis in animals and, by extrapolation, to man. Through a better understanding, we should hopefully be better able to prevent and treat the disease process and thus make inroads into this segment of patients who eventually develop end stage renal disease. In view of the enormous personal, social and financial cost of end stage renal disease secondary to GN in today's society, the benefits of better knowledge of the pathogenesis of the disease is self evident.